Memoirs Step 1 : Day 3
Argh another sucky day!
i think I am losing my head here. I need to focus.
Beijing time 22 :18 pm
Increased plasma Ca++ levels stimulus for release
Secreted by para-follicular C cells of thyroid.
Decreases the activity of osteoclasts and hence decreases serum calcium
* Take away point.. UNDER PATHO-PHYSIOLOGICAL CONDITIONS CALCITONIN HAS LITTLE IMPACT ON CONTROLLING OF SERUM CALCIUM
That means any if you remove the thyroid , or have a MEN syndrome related to parafollicular cells.. serum calcium will NOT be affected...
Vitamin D Metabolism
*Synthesized in skin by UV light.
*Ingested in food.
* Converted by hydroxylation in the liver to 25 OH form.
Clinical Pearl : Since the body stores of vitamin D are in liver, checking serum 25 OH levels are the best measure of body stores of vitamin D instead of active vitamin D hormone.
* Converted in the kidneys to 1,25 di hydroxy vitamin D or active vitamin D
Stimulus for Secretion of Vitamin D
* Low serum Ca++ levels
* Low serum Phosphorus levels
* Increased PTH levels
Actions of Vitamin D
* There is increased reabosorption of intestinal Ca++ and P from the intestine
* There is increased distal tubular reabsorotpion of calcium
* Bone is deposited ------- Because rise of serum Ca and P causes due to intestinal absorption INCREASES their product to more than Solubility product
* Note: An abnormally high vitamin D3 on the other hand, causes bone resorption ----> by activating osteoclasts and acting synergestically with PTH horomne.
Disorders of Calcium and Phosphate Metabolism
There are a couple of ways to look at this:
1. Primary Hyperparathyroidism
Drive in Point : Any time you see increased serum PTH and increased serum calcium,
think blindly of primary hyperparathyroidism..
* Initiating factor for this is increased serum PTH
* Labs : increased serum Ca++ , decreased serum P, increased urine calcium (calciuria) and polyuria, increased bone ALP, increased urinary cAMP and hydroxyproline
* Others : Decreased bone mass
Clinical Pearl : Decreased bone mass will be a feature of all hypercalcemic states except milk-alkali syndrome
* Symptoms : lethargy, fatigue, depression , concentrating difficulty
2. Secondary Hyperparathyroidism
Drive in Point : Any time the PTH levels are rising and plasma calcium is low ,
think of 2 diseases
Secondary hyperparathyroidism ( due to chronic renal failure)
End-organ resistance to action of PTH.
PTH will be high as in secondary hyper and calcium will be low.. )
*Due to renal failure, serum P will also be low
and the storage form of vitamin D 25 OH levels will be low, as no active vitamin D3 can be formed in proximal tubules of the kidney which is diagnostic .
Very Imporant : In the USMLE, they will throw in a question with same labs .. as above
How to differentiate pseduohypo state from secondary hyperparathyroidism
Both have increased PTH
Both have low Calcium and low Phosphorus ( due to renal failure and lack of Gs protein action in kidney )
Both will have decreased levels of storage 25 OH levels.
They will give a clue to differentitate: They will talk about a mental retardation , short and stocky stature, missing 4th or 5th metacarpals )
Yes , you got it .. Albright's hereditary dystrophy or type 1a pseudohypoparathyroidism
Yes they are other types, but they will not be tested on the USMLE examination.
3. Tertiary Hyperparathyroidism
A condition in which the parathyroids after prolonged stimulation are no longer under the control of body's homeostatic mechanisms
And become autonomous.
Whenever they mention autonomous you can assume it's tertiary form of hyperparathyroidism
I guess that covers the hyperparathyroid states.
Oh yes, note that serum calcium can be low or high in hyperparathyroidism...
Its the PTH levels that decides if it's primary or secondary : )
I did the same thing today! Ha!
Primary Disorder: Calcium and Phosphate change in opposite direction. (CRF is the only exception.)
Secondary Disorder: Calcium and Phosphate will change in the same direction.
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